ArticleAutoimmunity2008
Recombinant cardiac myosin fragment induces experimental autoimmune myocarditis via activation of Th1 and Th17 immunity.
Article in Autoimmunity, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 49 citations in OpenAlex.
- Hyperbaric Oxygen Therapy in Experimental Autoimmune Myocarditis: Insights from Preclinical Models to Translational Perspectives.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- T cells in cardiac health and disease.The Journal of clinical investigation · 2025Review
- Review
- The Molecular Role of Immune Cells in Dilated Cardiomyopathy.Medicina (Kaunas, Lithuania) · 2023Review
- Modulation of NRF-2 Pathway Contributes to the Therapeutic Effects ofAntioxidants (Basel, Switzerland) · 2022Article
- IgG2 rules: N-acetyl-β-D-glucosamine-specific IgG2 and Th17/Th1 cooperation may promote the pathogenesis of acute rheumatic heart disease and be a biomarker of the autoimmune sequelae ofFrontiers in cardiovascular medicine · 2022Article
- Focus on Autoimmune Myocarditis in Graves' Disease: A Case-Based Review.Frontiers in cardiovascular medicine · 2021Review
- A Case of Autoimmune Myocarditis Treated with IL-17 Inhibition.Kansas journal of medicine · 2021Article
- Viral myocarditis involves the generation of autoreactive T cells with multiple antigen specificities that localize in lymphoid and non-lymphoid organs in the mouse model of CVB3 infection.Molecular immunology · 2020Article
- Deficiency of Phospholipase AInflammation · 2020Article
- Galectin-3 deficiency enhances type 2 immune cell-mediated myocarditis in mice.Immunologic research · 2018Article
- Article
- Targeted Therapy for Acute Autoimmune Myocarditis with Nano-Sized Liposomal FK506 in Rats.PloS one · 2016Article
- Depletion of regulatory T cells decreases cardiac parasitosis and inflammation in experimental Chagas disease.Parasitology research · 2015Article
- A DPP-4 inhibitor suppresses fibrosis and inflammation on experimental autoimmune myocarditis in mice.PloS one · 2015Article
- Rethinking Molecular Mimicry in Rheumatic Heart Disease and Autoimmune Myocarditis: Laminin, Collagen IV, CAR, and B1AR as Initial Targets of Disease.Frontiers in pediatrics · 2014Article
- Article
- Paricalcitol reduces peritoneal fibrosis in mice through the activation of regulatory T cells and reduction in IL-17 production.PloS one · 2014Article
- STAT3 activity is necessary and sufficient for the development of immune-mediated myocarditis in mice and promotes progression to dilated cardiomyopathy.EMBO molecular medicine · 2013Article
- Pathogenesis of chagas' disease: parasite persistence and autoimmunity.Clinical microbiology reviews · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The specificity and function of T helper (Th) immune responses underlying the induction, progression, and resolution of experimental autoimmune myocarditis (EAM) in A/J mice are unclear. Published data suggest involvement of both Th1 and Th2 responses in EAM; however, the previous inability to assess antigen-specific in vivo and in vitro T-cell responses in cardiac myosin-immunized animals has confounded our understanding of this important model of autoimmune myocarditis. The goal of our study was to develop an alternative model of EAM based on a recombinant fragment of cardiac myosin, in hopes that the recombinant protein will permit measurement of functional T-cell responses that is not possible with purified native protein. A/J mice immunized with a recombinant fragment of cardiac myosin spanning amino acids 1074-1646, termed Myo4, developed severe myocarditis characterized by cardiac hypertrophy, massive mononuclear cell infiltration and fibrosis, three weeks post-immunization. The mice also developed an IgG1 dominant humoral immune response specific for both Myo4 and purified cardiac myosin. The in vitro stimulation of splenocytes harvested from Myo4-immunized animals with Myo4 resulted in cellular proliferation with preferential production of the Th1- and Th17-associated cytokines, IFN-gamma, IL-17, and IL-6, respectively. Production of IL-4 was negligible by comparison. This study describes a new model of EAM, inducible by immunization with a specific fragment of cardiac myosin, from which antigen-specific analyses reveal an importance for both Th1 and Th17 immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.